Development and validation of a predictive model for stroke associated pneumonia in patients after thrombectomy for acute ischemic stroke.

Objective: This study aims to identify the risk factors associated with stroke-associated pneumonia (SAP) in patients who have undergone thrombectomy for acute ischemic stroke and to develop a nomogram chart model for predicting the occurrence of pneumonia. Methods: Consecutive patients who underwent thrombectomy for acute ischemic stroke were enrolled from three hospitals at Taizhou Enze Medical Center. They were randomly divided into a training group and a validation group in a 7:3 ratio. The training group data was used to screen for effective predictive factors using LASSO regression. Multiple logistic regression was then conducted to determine the predictive factors and construct a nomogram chart. The model was evaluated using the validation group, analyzing its discrimination, calibration, and clinical decision curve. Finally, the newly constructed model was compared with the AIS-APS, A2DS2, ISAN, and PANTHERIS scores for acute ischemic stroke-associated pneumonia. Results: Out of 913 patients who underwent thrombectomy, 762 were included for analysis, consisting of 473 males and 289 females. The incidence rate of SAP was 45.8%. The new predictive model was constructed based on three main influencing factors: NIHSS ≥16, postoperative LMR, and difficulty swallowing. The model demonstrated good discrimination and calibration. When applying the nomogram chart to threshold probabilities between 7 and 90%, net returns were increased. Furthermore, the AUC was higher compared to other scoring systems. Conclusion: The constructed nomogram chart in this study outperformed the AIS-APS, A2DS2 score, ISAN score, and PANTHERIS score in predicting the risk of stroke-associated pneumonia in patients with acute ischemic stroke after thrombectomy. It can be utilized for clinical risk prediction of stroke-associated pneumonia in patients after thrombectomy for acute ischemic stroke.

Tanreqing suppresses the proliferation and migration of non-small cell lung cancer cells by mediating the inactivation of the HIF1α signaling pathway via exosomal circ-WDR78.

Circular RNAs (circRNAs) have emerged as regulators of cancer progression, including non-small cell lung cancer (NSCLC). Tanreqing (TRQ), a traditional Chinese medicine, is used clinically for respiratory diseases. RT-qPCR quantified circ-WDR78 expression in NSCLC cells. Cell growth, apoptosis, invasion, and migration were assessed by functional assays. RNA-binding protein immunoprecipitation (RIP), luciferase reporter, and RNA pull-down assays determined the competing endogenous RNA (ceRNA) network of circ-WDR78. The interaction between HIF1α and CD274 (PD-L1) promoter was analyzed by chromatin immunoprecipitation (ChIP). Circ-WDR78 expression was up-regulated in TRQ-treated NSCLC cells. Functionally, circ-WDR78 exhibited anti-tumor effects in these cells. Additionally, circ-WDR78 could also induce reactive oxygen species (ROS) accumulation by down-regulating HIF1α expression, promoting autophagy. Mechanistically, circ-WDR78 destabilizes HIF1α via the miR-1265/FBXW8 axis. TRQ-induced exosome secretion from NSCLC cells inhibits PD-L1 expression, preventing immune escape. We found that TRQ-treated NSCLC cells secrete exosomes to transmit circ-WDR78 to untreated NSCLC cells, inhibiting the malignancy of recipient tumor cells. In conclusion, TRQ inhibits NSCLC cell proliferation, invasion, and migration through exosomal circ-WDR78-mediated inactivation of the HIF1α signaling pathway, providing potential insight into TRQ injection for NSCLC treatment.Communicated by Ramaswamy H. Sarma.

Polarization-Insensitive Transmissive Metasurfaces Using Pancharatnam-Berry and Resonant Phases in Microwave Band.

Most of the existing metasurfaces are effective for the incident wave with the specific circularly polarized (CP) or linearly polarized (LP) state, that is the polarization-sensitive metasurface. This drawback dramatically hinders the practical use of the metasurface. Herein, this paper presents a strategy of polarization-insensitive transmissive microwave metasurfaces to manipulate the incident wave with arbitrary CP and LP states. The metasurface consists of polarization-insensitive unit cells. For the left circularly polarized (LCP) and right circularly polarized (RCP) incident waves, the same abrupt phase covering 0° to 360° can be realized by combining the Pancharatnam-Berry (PB) and resonant phases. As the arbitrary LP wave can decompose into the LCP and RCP waves, metasurfaces consisting of designed unit cells are valid for any polarization states. The polarization-insensitive transmissive microwave metalens and orbital angular momentum multiplexing metasurface working at 23 GHz are devised for verification. Simulation and measurement results verify the availability of the approach. The proposed method is suitable for designing microwave-transmissive metasurfaces capable of polarization insensitivity.

Treatment failure in a patient infected with Listeria sepsis combined with latent meningitis: A case report.

BACKGROUND: Listeria is a food-borne disease, which is rarely prevalent in the normal population; it mostly occurs in pregnant women, newborns, immunodeficiency patients, and the elderly. The main manifestations of this disease in patients include sepsis, meningitis, etc, and the mortality rate remains high, although the onset of meningitis is relatively insidious. CASE SUMMARY: A 75-year-old man presented with a fever for 1 wk and was admitted to the hospital for diagnosis and management of a lung infection. His condition improved after receiving anti-infective treatment for 2 wk. However, soon after he was discharged from the hospital, he developed fever again, and gradually developed various neurological symptoms, impaired consciousness, and stiff neck. Thereafter, through the cerebrospinal fluid metagenomic testing and blood culture, the patient was diagnosed with Listeria monocytogenes meningitis and sepsis. The patient died after being given active treatment, which included penicillin application and invasive respiratory support. CONCLUSION: This case highlights the ultimate importance of early identification and timely application of the various sensitive antibiotics, such as penicillin, vancomycin, meropenem, etc. Therefore, for high-risk populations with unknown causes of fever, multiple blood cultures, timely cerebrospinal fluid examination, and metagenomic detection technology can assist in confirming the diagnosis quickly, thereby guiding the proper application of antibiotics and improving the prognosis.

Corynoline Alleviates Osteoarthritis Development via the Nrf2/NF-κB Pathway.

Purpose: OA is a multifactorial joint disease in which inflammation plays a substantial role in the destruction of joints. Corynoline (COR), a component of Corydalis bungeana Turcz., has anti-inflammatory effects. Materials and Methods: We evaluated the significance and potential mechanisms of COR in OA development. The viabilities of chondrocytic cells upon COR exposure were assessed by CCK-8 assays. Western blot, qPCR, and ELISA were used to assess extracellular matrix (ECM) degeneration and inflammation. The NF-κB pathway was evaluated by western blot and immunofluorescence (IF). Prediction of the interacting proteins of COR was done by molecular docking, while Nrf2 knockdown by siRNAs was performed to ascertain its significance. Micro-CT, H&E, Safranin O-Fast Green (S-O), toluidine blue staining, and immunohistochemical examination were conducted to assess the therapeutic effects of COR on OA in destabilization of medial meniscus (DMM) models. Results: COR inhibited ECM degeneration and proinflammatory factor levels and modulated the NF-κB pathway in IL-1ß-treated chondrocytes. Mechanistically, COR bound Nrf2 to downregulate the NF-κB pathway. Moreover, COR ameliorated the OA process in DMM models. Conclusion: We suggest that COR ameliorates OA progress through the Nrf2/NF-κB axis, indicating COR may have a therapeutic potential for OA.

RAPID Software to the Clinical Application Value of Acute Basilar Artery Occlusion with Endovascular Treatment.

OBJECTIVE: To investigate the clinical application value of RAPID software based on computed tomography perfusion imaging (CTP) in the endovascular treatment of acute basilar artery occlusion (BAO). MATERIALS AND METHODS: The data of patients with acute basilar artery occlusion who received endovascular treatment in Taizhou Hospital, Zhejiang Province, between January 2020 and April 2021 were retrospectively analysed. The patients were divided into a perfusion imaging and a no-perfusion imaging group based on whether the image analysis results were obtained by RAPID software. Age, preoperative National Institute of Health stroke scale (NIHSS) score, onset to puncture time (OPT), operation methods, good prognosis at 3 months after surgery (modified Rankin scale (mRS) score ≤3), symptomatic intracranial haemorrhage (sICH) and other clinical data were compared between the two groups. Multivariate logistic regression analysis was used to identify the independent factors affecting the prognosis of BAO patients. RESULTS: In total, 61 patients with acute BAO were included: 31 patients in the perfusion imaging group and 30 patients in the no-perfusion imaging group. There were no statistically significant differences between the two groups in age, NIHSS score or operation methods (all P >0.05). However, OPT and the good prognosis rate were significantly higher in the perfusion imaging group than in the no-perfusion imaging group (χ2=8.176, 5.003, P < 0.05). SICH was significantly lower in the perfusion imaging group than in the no-perfusion imaging group (χ2=5.628, P < 0.05). Logistic regression analysis showed that the image analysis results of RAPID software influenced the prognosis of EVT in patients with acute BAO (OR=4.048, 95%CI: 1.276-12.840). CONCLUSIONS: RAPID software based on CTP can be used for preoperative screening of patients with acute basilar artery occlusion to identify those suitable for endovascular treatment, which is worthy of clinical promotion.

MMP-10 rs17435959 Polymorphism is Associated with the Formation and Stability of Carotid Atherosclerosis Plaque: A Case-Control Study.

BACKGROUND: Matrix metalloproteinase 10 (MMP-10) has a close relationship with carotid atherosclerosis (CAS) and cerebral infarction. The MMP-10 rs17435959 polymorphism causes a leucine to valine transition at codon 4 in exon 1 of the MMP-10 gene and may have functional effects. OBJECTIVES: To investigate the relationship between the MMP-10 rs17435959 polymorphism and the formation and stability of CAS plaques. MATERIALS AND METHODS: The present case-control study contains 738 visitors who came to our health examination center for the first time. According to the carotid ultrasound examinations, visitors were classified into the vulnerable plaque group (41-86 years old, 141 male, 105 female), the stable plaque group (41-86 years old, 141 male, 105 female) and the no plaque group (41-85 years old, 141 male, 105 female). All visitors in the three groups were sex- and- age-matched, and cardiovascular and cerebrovascular diseases were absent. The polymorphism was genotyped by real-time polymerase chain reaction- restriction. RESULTS: Compared to the GG genotype, the frequency of the CC and CG genotypes was significantly more common in the vulnerable plaque group than in the no plaque group (18.7% vs. 7.7%, unadjusted P = 0.002). Moreover, compared to the G allele, the frequency of the C allele was significantly more common in the vulnerable plaque group than in the no plaque group (10.4% vs. 3.9%, unadjusted P = 0.000) and in the vulnerable plaque group than in the stable plaque group (10.4% vs. 5.1%, unadjusted P = 0.008). Binary logistic regression showed that the CC and CG genotype was independent risk factor for the formation (P = 0.019, OR = 1.961, 95% CI [1.117, 3.444]) and vulnerability (P = 0.035, OR = 1.842, 95% CI [1.045, 3.247]) of CAS plaques. Moreover, individuals who have the C allele showed a higher level of fibrinogen, which was an independent risk factor for the formation of CAS plaques (P = 0.000, OR = 2.425, 95% CI [1.475, 3.985]). CONCLUSIONS: The rs17435959 polymorphism was associated with the formation and vulnerability of CAS plaques. Individuals who had variant-type MMP-10 showed higher levels of fibrinogen, which promoted the formation of CAS plaques.

circHIPK3 Acts as Competing Endogenous RNA and Promotes Non-Small-Cell Lung Cancer Progression through the miR-107/BDNF Signaling Pathway.

Circular RNAs (circRNAs) act as a crucial part in many human diseases, particularly in cancers. circRNA HIPK3 (circHIPK3) is a special circRNA that may participate in the oncogenesis of non-small-cell lung cancer (NSCLC), even though its latent regulatory mechanism is not very clear. Here, we studied the roles of circHIPK3 in NSCLC. qRT-PCR assay was applied to study the expression of circHIPK3 in NSCLC. The influence of circHIPK3 on NSCLC was estimated by silencing circHIPK3 and miR-107 mock transfection and brain-derived neurotrophic factor (BDNF) overexpression, and the correlation between circHIPK3, miR-107, and BDNF was evaluated by dual-luciferase reporter assay. The results showed that circHIPK3 expression was upregulated in NSCLC cells. circHIPK3 knockdown inhibited the migration and proliferation of NSCLC cells by promoting the expression of miR-107. circHIPK3 could be used as a miR-107 sponge to promote BDNF cell proliferation. The dual-luciferase reporter assay proved that miR-107 was the target of circHIPK3, and miR-107 had an interaction with the 3'untranslated region of BDNF. miR-107 overexpression inhibited BDNF-mediated NSCLC cell proliferation. These results indicate that circHIPK3 promotes tumor progression through a new circHIPK3/miR-107/BDNF axis, which offers potential markers and medical treatment for NSCLC.

SRCIN1 Regulated by circCCDC66/miR-211 Is Upregulated and Promotes Cell Proliferation in Non-Small-Cell Lung Cancer.

The incidence and mortality of lung cancer were extremely high. The present study showed that SRCIN1 was an oncogene in non-small-cell lung cancer (NSCLC). Public dataset analysis showed SRCIN1 was significantly overexpressed in NSCLC samples. Also, we found that NSCLC patients with higher SRCIN1 expression had shorter OS time by analyzing TCGA, Kaplan-Meier Plotter, GSE30219, GSE50081, and GSE19188 databases. Overexpression or knockdown of SRCIN1 significantly induced or reduced A549 and H1299 cell proliferation. Furthermore, we found SRCIN1 was directly targeted by miR-211. Overexpression or knockdown of miR-211 suppressed or induced SRCIN1 levels in NSCLC. Moreover, we found that miR-211 affected NSCLC cell proliferation through SRCIN1. Previous studies demonstrated that circRNAs could act as miRNA sponges in cancer cells. In this study, we showed that knockdown of circCCDC66 induced expression of miR-211. Luciferase assay demonstrated that miR-211 suppressed the activity of luciferase reporter-contained circCCDC66 sequences. Moreover, knockdown of circCCDC66 significantly inhibited SRCIN1 levels in both A549 and H1299 cells. These results showed that circCCDC66 acted as a miRNA sponge to affect the miR-211/SRCIN1 axis. Of note, we for the first time revealed that circCCDC66 suppression reduced cell proliferation by about 65% in A549 and by about 40% in H1299 cells. We thought this study could provide novel potential biomarkers for NSCLC.

Circular RNA circ-CPA4/ let-7 miRNA/PD-L1 axis regulates cell growth, stemness, drug resistance and immune evasion in non-small cell lung cancer (NSCLC).

BACKGROUND: Non-small cell lung cancer (NSCLC) cells derived intracellular and extracellular programmed cell death ligand 1 (PD-L1) promoted cancer progression and drug resistance, and facilitated tumor immune evasion. However, the detailed molecular mechanisms are still largely unknown. In the present study, we aimed to explore the role of circular RNA circ-CPA4/let-7 miRNA/PD-L1 axis in the regulation of NSCLC progression, drug resistance and tumor immune microenvironment. METHODS: Real-Time qPCR and Western Blot analysis were conducted to examine gene expressions at transcriptional and translated levels, respectively. The regulatory mechanisms of circ-CPA4, let-7 miRNA and PD-L1 were validated by dual-luciferase reporter gene system and RNA pull-down assay. Cell growth and apoptosis were determined by CCK-8 assay, colony formation assay and Annexin V-FITC/PI double staining assay. Cell mobility was evaluated by transwell assay. RESULTS: Circ-CPA4 and PD-L1 were high-expressed, while let-7 miRNA was low-expressed in NSCLC cells and cancer tissues compared to the human bronchial epithelial (HBE) cells and their paired clinical normal adjacent tissues, respectively. Besides, knock-down of circ-CPA4 inhibited cell growth, mobility and epithelial-mesenchymal transition (EMT), and promoted cell death in NSCLC cells by downregulating PD-L1 through serving as a RNA sponge for let-7 miRNA. In addition, the NSCLC cells derived PD-L1-containing exosomes promoted cell stemness and increased resistance of NSCLC cells to cisplatin. Notably, by co-culturing the NSCLC cells with CD8+ T cells isolated from human peripheral blood mononuclear cells (hPBMCs) in a transwell co-culturing system, we found that NSCLC cells inactivated CD8+ T cells in a secreted PD-L1-dependent manner. Further results suggested that circ-CPA4 also positively regulated exosomal PD-L1, and the NSCLC cells with circ-CPA4 ablation re-activated CD8+ T cells in the co-culturing system. CONCLUSION: Taken together, circ-CPA4 regulated cell growth, mobility, stemness and drug resistance in NSCLC cells and inactivated CD8+ T cells in the tumor immune microenvironment through let-7 miRNA/PD-L1 axis.

Circular RNA circ-LDLRAD3 serves as an oncogene to promote non-small cell lung cancer progression by upregulating SLC1A5 through sponging miR-137.

Circular RNAs (circRNAs) are closely associated with the development of non-small cell lung cancer (NSCLC); however, it is still unclear whether circular RNA circ-LDLRAD3 participated in the regulation of NSCLC progression. In this study, we found that circ-LDLRAD3 was high-expressed and miR-137 was low-expressed in NSCLC tissues and cells compared to their normal counterparts, which showed negative correlations in NSCLC tissues. Further experiments validated that miR-137 could be sponged and inhibited by circ-LDLRAD3 in NSCLC cells. In addition, knock-down of circ-LDLRAD3 and miR-137 overexpression promoted NSCLC cell apoptosis, and inhibited cell proliferation and invasion. Similarly, upregulation of circ-LDLRAD3 or miR-137 ablation had opposite effects on the above cell functions. Besides, the glutamine transporter SLC1A5 was validated to be the downstream target of circ-LDLRAD3 and miR-137, and upregulated circ-LDLRAD3 increased SLC1A5 expression levels by downregulating miR-137. Furthermore, the effects of downregulated circ-LDLRAD3 on cell proliferation, apoptosis and mobility were all reversed by knocking down miR-137 and overexpressing SLC1A5. Taken together, this in vitro study found that knock-down of circ-LDLRAD3 inhibited the development of NSCLC by regulating miR-137/SLC1A5 axis.

YY1-induced lncRNA ZFPM2-AS1 facilitates cell proliferation and invasion in small cell lung cancer via upregulating of TRAF4.

BACKGROUND: Newly identified lncRNA zinc finger protein, FOG family member 2 antisense RNA 1 (ZFPM2-AS1) is identified as an oncogenic gene. However, the role of ZFPM2-AS1 in small cell lung cancer (SCLC) is poorly comprehended. METHODS: The expression of genes in SCLC tissues and cells was measured by qRT-PCR. Colony formation, EdU, CCK-8, transwell and wound healing as well as in vivo assays revealed the function of ZFPM2-AS1 in SCLC. ChIP, luciferase reporter, RIP and RNA pull down assays demonstrated the binding relation among genes. RESULTS: ZFPM2-AS1 was significantly upregulated in SCLC tissues and cells. ZFPM2-AS1 deficiency attenuated SCLC cell proliferation, invasion and migration. In addition, ZFPM2-AS1 was transcriptionally activated by Yin Yang 1 (YY1) factor. Further, miR-3612 was confirmed as downstream miRNA of ZFPM2-AS1. Moreover, TNF receptor associated factor 4 (TRAF4) was the target gene of miR-3612 in SCLC. ZFPM2-AS1, miR-3612 and TRAF4 jointly constituted a competing endogenous RNA (ceRNA) network in SCLC. Finally, TRAF4 could countervail ZFPM2-AS1 downregulation-mediated function on SCLC cell proliferation and invasion in vitro and tumor growth in vivo. CONCLUSION: Our study elucidated the oncogenic effect of ZFPM2-AS1 in SCLC progression, indicating it may be a therapeutic target for SCLC.

MYORG Mutation Heterozygosity Is Associated With Brain Calcification.

BACKGROUND: Biallelic mutations in the MYORG gene were first identified as the cause of recessively inherited primary familial brain calcification. Interestingly, some heterozygous carriers also exhibited brain calcifications. OBJECTIVES: To further investigate the role of single heterozygous MYORG mutations in the development of brain calcifications. METHODS: A nation-wide cohort of Chinese primary familial brain calcification probands was enrolled from March 2016 through September 2019. Mutational analysis of MYORG was performed in 435 primary familial brain calcification probands who were negative for mutations in the other four known primary familial brain calcification-causative genes (SLC20A2, PDGFRB, PDGFB, and XPR1). RESULTS: Biallelic MYORG mutations were identified in 14 primary familial brain calcification patients from 10 unrelated families. Interestingly, 12 heterozygous carriers from seven of these families also exhibited mild-to-moderate brain calcifications. Moreover, single heterozygous mutations were detected in an additional 9 probands and in 7 of their family members affected with brain calcifications. In our cohort, clinical and imaging penetrance of individuals with biallelic mutations were 100%, whereas among individuals with heterozygous mutations, penetrance of imaging phenotype was reduced to 73.7% (28 of 38) and clinical penetrance was much lower. Most (34 of 38) remained asymptomatic whereas 4 carriers had symptoms of uncertain clinical significance (nonspecific depression, epilepsy and late-onset parkinsonism). Compared with individuals with biallelic MYORG mutations, individuals with heterozygous mutations had brain calcifications with much lower calcification scores (P < 2e-16). CONCLUSIONS: Presence of brain calcifications in individuals with heterozygous MYORG mutations suggested a semidominant inheritance pattern with incomplete penetrance. This finding further expanded the genotype-phenotype correlations of MYORG-related primary familial brain calcification. © 2020 International Parkinson and Movement Disorder Society.

Association of Crohn's Disease with Aryl Hydrocarbon Receptor Gene Polymorphisms in Patients from Southeast China.

Aims The aryl hydrocarbon receptor (AhR) plays a pivotal role in regulating the innate and the acquired immune systems. The present study aimed to investigate the association of Crohn's disease (CD) with AhR polymorphisms in a cohort of patients from Southeast China. Methods An improved multiple ligase detection reaction technique was applied to examine the polymorphisms of rs2158041, rs2066853, and rs10249788 in 310 patients with CD and 573 controls. Results Compared to the controls, the variant allele (T) and genotype (CT+TT) of rs2158041 were less frequent in patients with CD (both p < 0.05). Similar conclusions were drawn from patients with ileal CD and with stricture CD as compared to the controls (all p < 0.0083). However, no significant differences were observed in allele and genotype frequencies of rs2066853 and rs10249788 between patients with CD and the controls (all p > 0.05). Although rs2158041 and rs10249788 were in complete linkage disequilibrium with rs2066853, respectively, only the frequency of haplotype (TG) formed by rs2158041 and rs2066853 was significantly lower in patients with CD than that in the controls (p < 0.05). Conclusions AhR (rs2158041) might be a susceptible locus for CD, especially for the two subtypes: ileal CD and stricture CD.

Association of Ulcerative Colitis with FOXP3 Gene Polymorphisms and Its Colonic Expression in Chinese Patients.

Abnormalities of forkhead box P3 (FOXP3) are implicated in various autoimmune diseases. This study is aimed at investigating the association of ulcerative colitis (UC) with FOXP3 polymorphisms and its colonic expression in Chinese patients. Polymorphisms of rs3761548, rs2232365, rs2294021, and rs3761547 were examined in 472 UC patients and 525 healthy controls using the SNaPshot method. The colonic expression of FOXP3 mRNA and protein was assayed in inflammatory mucosa of 34 UC patients and normal mucosa of 36 patients with benign sigmoid polyps (normal controls) using real-time quantitative polymerase chain reaction and immunohistochemical analysis. All data were handled separately for females and males. As a result, the carrier frequencies with at least one variant allele of rs3761548, rs2232365, and rs229402 increased in female and male UC patients compared with healthy controls. Significant differences in these carrier frequencies were also observed between patients with mild and moderate UC and patients with severe UC. The expression of FOXP3 was higher in UC patients (both males and females), especially those with severe UC, than in normal controls. The expression of FOXP3 was downregulated in UC patients having at least one variant allele compared with UC patients having no variant allele of rs3761548, rs2232365, and rs2294021. Male gender (ß = -0.341), rs2294021 variation (ß = -0.503), and severe UC (ß = 0.361) were independently related to the mRNA expression of FOXP3 in UC patients. Together, our findings indicated that FOXP3 (rs3761548, rs2232365, and rs2294021) variations increased the risk of UC and were associated with the lower colonic expression of FOXP3 in UC patients.

Reconfigurable Multifunctional Metasurface Hybridized with Vanadium Dioxide at Terahertz Frequencies.

Driven by the continuous demand for system integration and device miniaturization, integrating multiple diversified functions into a single metasurface hybridized with the tunable metaparticle is highly demanding at terahertz (THz) range. However, up to now, because of the limitation of the tunable metaparticle at terahertz range, most of the metasurfaces feature a single function only or process similar functionalities at a single frequency. A reconfigurable multifunctional metasurface which can realize the switch of transmission and reflection and manipulate the linearized polarization state of electromagnetic waves simultaneously over a controllable terahertz frequency range based on the vanadium dioxide was designed for the first time in the paper. The numerical result demonstrates the validity of the appropriately designed metasurface. Simulation results show that the reconfigurable and multifunctional performance of this metasurface can be acquired over 1.59 THz to 1.74 THz without re-optimizing or re-fabricating structures, which effectively extends the operating frequencies. The proposed metasurface holds potential for electromagnetic wave manipulation and this study can motivate the realization of the wideband multifunctional metasurface and the software-driven reconfigurable metasurface at terahertz frequencies.

A Case-Control Study on Association of Ulcerative Colitis with FCGR2A Gene Polymorphisms in Chinese Patients.

BACKGROUND AND AIMS: The Fc gamma receptor IIa (FcγRIIa), encoded by FCGR2A gene, has been suggested to play a crucial role in immunity by linking immunoglobulin G antibody-mediated responses with cellular effector and regulatory functions. Polymorphisms in FCGR2A have been shown to affect FcγRIIa/antibody interactions and have been potentially implicated in several autoimmune and inflammatory conditions. This study was designed to analyze the association between ulcerative colitis (UC) and FCGR2A polymorphisms in the Chinese population. MATERIALS AND METHODS: A total of 422 patients with UC and 710 unaffected controls were recruited. Five single nucleotide polymorphisms of FCGR2A (rs1801274, rs10800309, rs4657039, rs511278, and rs6696854) were genotyped by SNaPshot. Analyses for linkage disequilibrium (LD) and haplotype studies of FCGR2A were performed for all study subjects. RESULTS: The frequency of the minor homozygote (CC) of the rs1801274 SNP of FCGR2A was shown to be significantly lower in patients with UC than in controls (7.1% vs. 12.1%, p = 0.008). Two haplotype blocks, formed by FCGR2A (rs4657039, rs6696854, and rs10800309) and FCGR2A (rs1801274 and rs511278), respectively, were observed in the subsequent LD analysis. The TC haplotype constructed by the major allele of FCGR2A (rs1801274 and rs511278) was more prevalent in UC patients compared with controls (65.2% vs. 60.2%, p = 0.017). CONCLUSIONS: The minor homozygote (CC) of FCGR2A (rs1801274) may contribute to decrease the susceptibility to UC and the TC haplotype formed by FCGR2A (rs1801274 and rs511278) may increase the risk of UC in the Chinese population.

Longitudinal evaluation of serum periostin levels in patients after large-artery atherosclerotic stroke: A prospective observational study.

Increasing evidence supports the involvement of periostin in the pathophysiological processes of stroke and atherosclerosis. The aim of this study was to assess circulating periostin levels at different times after large-artery atherosclerotic (LAA) stroke and their association with stroke. Serum periostin levels were measured using enzyme-linked immunosorbent assay on day 1 in 162 patients with LAA stroke and in 108 age- and sex-matched controls, on day 6 after stroke in 134 patients, and during the 4th week after stroke in 46 of the 162 patients. Stroke severity was determined using the National Institutes of Health Stroke Scale (NIHSS), and the stroke volume was measured. Outcome at 3 months was measured using the modified Rankin Scale (mRS). Our results indicated that periostin levels increased significantly on day 6 after stroke, and this increasing trend persisted for at least 4 weeks after the event. In addition, the increase in periostin levels was positively correlated with the NIHSS scores and stroke volume, but not with the mRS scores after adjusting for the NIHSS scores. In conclusion, these findings suggest that the increase in serum periostin levels observed after stroke may be associated with the stroke severity in patients with LAA stroke.

Control of the Spin Angular Momentum and Orbital Angular Momentum of a Reflected Wave by Multifunctional Graphene Metasurfaces.

Three kinds of multifunctional graphene metasurfaces based on Pancharatnam⁻Berry (PB) phase cells are proposed and numerically demonstrated to control a reflected wave’s spin angular momentum (SAM) and orbital angular momentum (OAM) in the terahertz (THz) regime. Each proposed metasurface structure is composed of an array of graphene strips with different deviation angles and a back-grounded quartz substrate. In order to further help readers have a deeper insight into the graphene-based metasurfaces, a detailed design strategy is also provided. With the aid of the designed graphene elements, the proposed metasurfaces can achieve the full 360° range of phase coverage and provide manipulation of SAM and OAM of a circularly polarized (CP) wave at will. More importantly, simultaneous control of these two momentums can also be realized, and in order to demonstrate this function, a THz spin-controlled OAM beam generator with diverse topological charges is created, which can provide one more degree of freedom to improve the channel capability without increasing the bandwidth compared to a linearly polarized (LP) OAM beam. Numerical results verify the proposed graphene metasurfaces, which pave the way for generating spin OAM vortex waves for THz communication systems.

Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis.

In mammals, oleic acid (OA) induces pulmonary edema (PE), which can initiate acute lung injury (ALI) and lead to acute respiratory distress syndrome (ARDS). Pulmonary surfactant (PS) plays a key role in a broad range of treatments for ARDS. The aim of the present investigation was to assess changes in the synthesis of phosphatidylcholine (PC) from choline and determine the effect of exogenous PS on its de novo synthesis in rats with OA-induced PE. Experimental rats were randomized into three groups, including a control group, OA-induced PE group, and OA-induced group treated with exogenous PS (OA-PS). Twenty-four rats were sacrificed 4 h after induction of the OA model, and tissue was examined by light and electron microscopy to assess the severity of ALI using an established scoring system at the end of the experiment. After 15 µCi 3H-choline chloride was injected intravenously, eight rats in each group were sacrificed at 4, 8, and 16 h. The radioactivity of 3H incorporated into total phospholipid (TPL) and desaturated phosphatidylcholine (DSPC) was measured in bronchoalveolar lavage fluid (BALF) and lung tissue (LT) using a liquid scintillation counter and was expressed as counts per minute (CPM). Results showed that TPL, DSPC, and the ratio of DSPC/total protein (TP) in lung tissue decreased 4 h after challenge with OA, but the levels recovered after 8 and 16 h. At 8 h after injection, 3H-TPL and 3H-DSPC radioactivity in the lungs reached its peak. Importantly, 3H-DSPC CPM were significantly lower in the PS treatment group (LT: Control: 62327 ± 9108; OA-PE: 97315 ± 10083; OA-PS: 45127 ± 10034, P < 0.05; BALF: Control: 7771 ± 1768; OA-PE: 8097 ± 1799; OA-PE: 3651 ± 1027, P < 0.05). Furthermore, DSPC secretory rate (SR) in the lungs was significantly lower in the PS treatment group at 4 h after injection (Control: 0.014 ± 0.003; OA-PE: 0.011 ± 0.004; OA-PS: 0.023 ± 0.006, P < 0.05). Therefore, we hypothesize that exogenous PS treatments may adversely affect endogenous de novo synthetic and secretory phospholipid pathways via feedback inhibition. This novel finding reveals the specific involvement of exogenous PS in endogenous synthetic and secretory phospholipid pathways during the treatment of ARDS. This information improves our understanding of how PS treatment is beneficial against ARDS and opens new opportunities for expanding its use.